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104 Liver and regulation metabolism > Lisa Mullen lectures MTT1 > Flashcards

Lisa Mullen lectures MTT1 Flashcards

biochemistry

1
Q

4 things energy is required for

A

> motion (muscle contraction)
transport (of ions/molecules across membranes)
biosynthesis of essential metabolites
thermoregulation

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2
Q

Why does Mg2+ deficiency make you feel tired

A

Mg2+ forms complex with ATP inside cells, deficiency impairs virtually all metabolism

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3
Q

A) What class of enzyme transfers electrons

B)What class of enzyme transfers functional groups

A

A) oxidoreductases

B) transferases

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4
Q

Which vitamin is needed for coenzyme:
A) FAD
B) NAD+

A

A) Riboflavin (B2)

B) Niacin

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5
Q

Glycolysis:

A) which enzyme phophorylates glucose into glucose-6-phosphate

B) Which enzyme is involved in the committed step, and what is the reaction

A

A) Hexokinase

B) PFK-1 catalyses fructose-6-phosphate into fructose 1,6 bisphosphate

*both priming reactions

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6
Q

Glycolysis:

Which reaction does Pyruvate kinase catalyse

A

phosphoenolpyruvate into pyruvate

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7
Q

Inside the mitochondria, what is the link reaction

include the enzyme that catalyses it

A

pyruvate + CoA + NAD+ ——-> acetyl CoA + NADH + H+

catalysed by PDH complex

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8
Q

Which 5 coenzymes make up PDH complex, and which 4 vitamins are vital for this complex

A

TPP, NAD+, CoA, FAD, Lipoic acid

Thiamine for TPP
Riboflavin for FAD
Niacin for NAD
Pantothenate for CoA

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9
Q

What does ACIKSSFMO stand for (order of intermediates in TCA cycle)

A 
Acetyl CoA
Citrate
Isocitrate
alpha-Ketoglutarate
Succinyl CoA
Succinate
Fumarate
L-Malate
Oxaloacetate
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10
Q

What are the two shuttles used to regenerate NAD+ via transport of 2 electrons

Where is each one mainly found

How many moles of ATP is produced

A

1) glycerol-3-phosphate shuttle, in brain and muscle
2) malate-aspartate shuttle, in liver and heart
1. 5 or 2.5 moles ATP

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11
Q

Which 4 complexes make up the ETC

Which soluble proteins link them

A

Complex I, II, III, IV

Linked by ubiquinone (coenzyme Q)
Cytochrome C (links III and IV)
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12
Q

Name the antiporter protein that transports ADP3- into matrix in exchange for ATP4- out of matrix

A

adenosine nucleotide translocase

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13
Q

Name of symporter that transports both phosphate and H+ into the matrix

A

phosphate translocase

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14
Q

2 functional domains of ATP synthase

A

Fo: an oligomycin-sensitive proton channel
F1: an ATP synthase

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15
Q

What is Atractyloside

A

found in thistle, specific inhibitor of adenosine nucleotide translocase

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16
Q

The different subunits that comprise Fo and F1 domains of ATP synthase

A

Fo: 13-15 a, b and c subunits

F1: 9 subunits of alpha 3, beta 3, gamma, delta and reverse E

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17
Q

2 uncoupling reagents that dissipate H+ gradient allowing H+ back into matrix via a diff route that is not ATP synthase, thus severing linnk between e- flow and ATP synthesis. Releasing energy as heat

A

occurs naturally: UCP1 (thermogenin): found in brown adipose tissue and has specific H+ chanel for H+ to flow back into matrix, releasing heat as it does so. Important in newborns to keep them warm

occurs unnaturally: DNP: a weight loss drug. A weak acid that crosses membranes ‘ferrying’ H+ across with it. Each DNP collects H+ from intemrembrane space, crosses inner membrane and deposits H+ in matrix. Can return to collect another proton

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18
Q

Compare nuclear and mitochondrial genome

A 
Nuclear:
Introns present
3% coding dna 
Histones associated
Maternal/paternal inheritance
20,000-30,000 genes encoded 
Mitochondrial genome:
no introns or histones
93% coding dna
Maternal inheritance only 
genes code for:
13 respiratory chain proteins
2 rRNA proteins
22 tRNA proteins (tRNA structure different)
19
Q

What are oxidative phosphorylation enzyme defects strongly associated with

A

alzheimers, parkinsons, type II diabetes

20
Q

heteroplasmy

A

presence of more than one type of mt DNA within a cell/ individual. It is important in determining the severity of diseases

21
Q

What is threshold effect

A

a disease will only present itself if 70% or more of mitochondria in a cell was mutant

22
Q

What does LHON stand for and what is it

A

Lebers hereditary optic neuropathy

single base change in mt gene ND4 (Arg>His) in complex I of ETC. Not enough ATP generated = damage to optic nerve = blindness

23
Q

What does MERRF stand for and what is it

A

Myoclonus epilepsy with ragged-red fibre

a point mutation in mt gene encoding tRNA specific for lysine, disrupts synthesis of proteins essential for OXPHOS = abnormal shaped mitochondria in skeletal muscle.

Ragged red fibres is red clumps of abnormal mitochondria that appears on staining

24
Q

What is MELAS syndrome, what does it stand for

>symptoms in childhood

A

Mitochondrial encephalomyopathy lactic acidosis

mt gene dysfunction effecting complex I and tRNA, effects brain and skeletal muscle

childhood symptoms: lactic acidosis, stroke-like symptoms with muscle weakness, seizures leading to loss of vision, involuntary muscle spasms (myoclonus), dementia

25
Q

What does KSS stand for and what is it

> symptoms

A

Kearns-sayre syndrome
results from 5kb deletion of mt genome, onset before 20
symptoms: dementia, retinitis pigmentosa

26
Q

mt myopathies treatment options

A

occupational/ physical therapy: may extend range of muscle movement

vitamin therapies: riboflavin, creatinine, CoQ, C, K and carnitine may help

27
Q

2 strategies to prevent mt myopathies

A

mitochondrial gene replacement (pronuclear stage)

maternal spindle transfer

28
Q

glucose is polar, so how enters cells via glucose transport proteins (gluts)
give 5 examples and where they are found

A

glut 1: found in erythrocytes, muscle, brain, kidney, colon, placenta

glut 2: found in liver, pancreatic cells

glut 3: found in brain

glut 4: found in skeletal muscle, adipose tissue

glut 5: small intestine (fructose transporter)

29
Q

Where does pentose phosphate pathway branch from

two products of pentose phosphate pathway And what they’re used for

A

Branches from glycolysis at G-6-P
Products:
1)ribose phosphate: used to synthesise RNA and DNA
2) NADPH: used for reductive biosynthesis and to maintain redox balance of cell

30
Q

what makes glycogen a GOOD energy store. What makes it a BAD energy store

A

GOOD: highly branched, large number of ends for phosphorylase and glycogen synthase to ensure rapid breakdown and resynthesis

BAD: glucose is hydrophillic, it associates with water increasing overall weight and bulk

31
Q

2 mechanisms of glycogenolysis

A

1) glycogen phosphorylase breaks bonds between alpha1,4 linked glucose by addition of phosphate to produce glucose-1-phosphate
2) alpha1,6 bonds requires debranching enzyme alpha1,6 glucosidase which is a hydrolysis reaction producing free glucose

32
Q

allosteric regulation of glycogen phosphorylase in muscle

A

AMP activates phosphorylase as it is a sign of ATP depletion

ATP and gluc-6-phosphate inhibit phosphorylase as they are a sign of inc energy levels

33
Q

allosteric regulation of glycogen synthase

A

activated by gluc-6-phosphate and ATP

In liver, glucose and G-6-P inhibits glycogenolysis

34
Q

How is glycogen phosphorylase activated by cAMP-dependent phosphorylation

What effect does this cAMP cascade have on glycogen synthase

A

cAMP cascade leads to phosphorylation of serine in glycogen phosphorylase, this activates glycogen phosphorylase. It is in ‘a’ conformation

opposite effect on glycogen synthase, it converts enzyme to ‘b’ conformation, the less active state

35
Q

what are main regulatory points for link reaction/ TCA cycle

A

link reaction: PDH complex

TCA cycle: citrate synthase, isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase

36
Q

anaplerotic reactions of TCA cycle

A

pyruvate replenishes OAA via pyruvate carboxylase

PEP replenishes OAA via PEP carboxylase

Malate is replenished by pyruvate into malate via malic enzyme

37
Q

Names of complex I,II,III and IV in ETC

A 
I = NADH dehydrogenase
II = succinate dehydrogenase
III = ubiquinone:cytochrome c oxidoreductase
IV= cytochrome oxidase
38
Q

theory of rotational catalysis

A

conformation 1: ADP+Pi are bound

conformation 2: ADP+Pi = ATP

conformation 3: ATP released (active site has low affinity for ATP in this formation)

39
Q

What is mitochondrial genetic bottleneck

A

The randomness in the way mitochondria is inherited specifically in the oocyte amplification and maturation stage means we can’t predict outcome of mitochondrial inheritance

39
Q

Functions of liver

A

Glycogen synthesis
Glycogenolysis
Gluconeogenesis
Fatty acid synthesis from glucose secrete as TAGs in VLDL
Synthesise ketone bodies and secretes into blood as fuel for other tissues
Stores fat soluble vitamins

40
Q

Why is brain most vulnerable to hypoglycaemia

A

1) cannot store glucose in significant amounts or synthesise glucose
2) cannot metabolise substrates other than glucose or ketone bodies
3) cannot extract sufficient glucose for their needs at low concentrations because glucose entry into brain is not facilitated by hormones

41
Q

Immediate and long term effects of insulin

A

Immediate:
Inc rate of glucose uptake in muscle and adipocytes
Modulation of activity of enzymes involved in glucose metabolism

Long term:
Inc expression of liver enzymes that synthesise glycogen
Inc expression of adipocyte enzymes that synthesise TGs, this inhibits lipolysis in adipose tissue
Functions as growth factor for some cells eg fibroblasts

42
Q

How is glycogen broken down in muscle vs liver

A

Muscle: glycogen >gluc 1 phosphate > gluc 6 phosphate > pyruvate > lactate +co2

Liver: glycogen >gluc 1 phosphate > gluc 6 phosphate > glucose via enzyme glucose 6 phosphatase

43
Q

How does glycogen form in first place

How do branches form

A

UDP-glucose donates first glucosyl residue and attaches it to aa tyrosine in protein glycogenin. Remaining glucose units added in alpha 1,4 linkage from UDP glucose creating growing chain

Branching enzyme transfers block of 7 residues to growing chain to create new branch with alpha 1,6 linkage. New branch cannot form within 4 residues of existing branch

104 Liver and regulation metabolism (5 decks)

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